About: P136 Combined action of type I and type III IFN restricts initial replication of SARS-coronavirus in the lung but fails to inhibit systemic virus spread

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About: P136 Combined action of type I and type III IFN restricts initial replication of SARS-coronavirus in the lung but fails to inhibit systemic virus spread Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	P136 Combined action of type I and type III IFN restricts initial replication of SARS-coronavirus in the lung but fails to inhibit systemic virus spread
Creator	Katze, M Miller, J Patel, J Fugier, E Gale, M Hoang, X Horner, S Immunology, Jouvin-Marche, E Krasnoselsky, A Leroy, V Manicassamy, B Marche, P Marlu, A Merad, M Sanchez Aparicio, M Sastre, A Schmolke, M Sturm, N Thélu, M.-A Van Campenhout, N Wilkins, C Zarski, J.-P
Source	Elsevier; PMC
abstract	Introduction STAT1-deficient mice are more susceptible to infection with SARS-Coronavirus (SARS-CoV) than type I IFN receptor-deficient mice. The increased susceptibility of STAT1-deficient mice is potentially due to the lack of functional type III IFN (IFN-λ) signalling. Methods We used mice lacking functional receptors for both type I and type III IFN (dKO) to evaluate the possibility that type III IFN plays a decisive role in SARS-CoV protection. Results We found that viral peak titres in lungs of dKO and STAT1-deficient mice were similar, although significantly higher than in wild-type mice. The kinetics of viral clearance from the lung was also comparable in dKO and STAT1-deficient mice. Surprisingly, however, infected dKO mice remained healthy, whereas infected STAT1-deficient mice developed liver pathology and eventually succumbed to neurological disease. Conclusion Our data suggest that the failure of STAT1-deficient mice to efficiently control initial SARS-CoV replication in the lung is due to impaired type I and type III IFN signaling, whereas the failure to control subsequent systemic viral spread is due to unrelated defects in STAT1-deficient mice.
has issue date	2012-09-30(xsd:dateTime)
bibo:doi	10.1016/j.cyto.2012.06.228
has license	els-covid
sha1sum (hex)	5d90fb7b571e9cfad48486c911796dbe9d917f33
schema:url	https://doi.org/10.1016/j.cyto.2012.06.228
resource representing a document's title	P136 Combined action of type I and type III IFN restricts initial replication of SARS-coronavirus in the lung but fails to inhibit systemic virus spread
has PubMed Central identifier	PMC7129343
schema:publication	Cytokine
resource representing a document's body	covid:5d90fb7b571e9cfad48486c911796dbe9d917f33#body_text
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